ライフサイエンスコーパス: helminth

1 injury after infection with a lung-migrating helminth.

2 fection, where they impact both the host and helminth.

3 eradication of pathogens, such as parasitic helminths.

4 nd public health control of soil-transmitted helminths.

5 tion in the lung in response to allergens or helminths.

6 one mechanism of EV biogenesis can occur in helminths.

7 e recombinant allergens that had homologs in helminths.

8 ith type 2 immune responses to allergens and helminths.

9 chronically infected with endemic parasitic helminths.

10 mune responses directed against allergens or helminths.

11 butions in reducing the global prevalence of helminths.

12 To explore this helminth/allergy interaction more fully, parasite- and a

13 ections with phylogenetic relatives of these helminths, also trematodes of the phylum Platyhelminthes

14 herpesviruses, influenza, and an intestinal helminth and compared their blood immune signatures to m

15 antibody production, thus protecting against helminthes and venoms.

16 Parasitic helminths and allergens induce a type 2 immune response

17 evidence of an inverse relationship between helminths and allergy-related outcomes, but strong evide

18 through which the immune system responds to helminths and an array of environmental substances such

19 gree of immunity against metazoan parasites (helminths and arthropods) in mammalian hosts.

20 ike cells and contribute to immunity to both helminths and fungi.

21 The interaction between helminths and gut bacteria is currently a subject of muc

22 ere, we review these studies and discuss how helminths and helminth-derived molecules may modulate th

23 y against coinfections with soil-transmitted helminths and Opisthorchis viverrini were secondary outc

24 lia including asthma, various skin diseases, helminths and reactions to medications.

25 , the responses induced by the extracellular helminths and those induced by the intracellular Mtb are

26 immune responses induced by infections with helminths and tuberculosis (TB) and then provide data fr

27 orrelated with pathogen diversity (bacteria, helminths) and prevalence of antibiotic-resistant urinar

28 cterial microbiota, their associated phages, helminthes, and fungi, which together constitute the mic

29 d to zoonotic parasites, including protozoa, helminths, and arthropods, may represent a major threat

30 tion in innate immune responses to parasitic helminths, and emerging evidence also indicates these ce

31 icrobes including bacteria, fungi, protozoa, helminths, and viruses.

32 imal DC phenotypic activation in response to helminth antigen (Ag), and efficient migration to, and l

33 We conclude that helminths are a small but important and potentially seve

34 Protozoa and helminths are members of the gut microbiota of mammals,

35 Parasitic helminths are potent immunomodulators and chronic infect

36 Intestinal helminths are potent regulators of their host's immune s

37 , and adverse effects in children in endemic helminth areas.

38 g feature of infection with parasitic worms (helminths), as well as being responsible for widespread

39 d in the intensity for the immune-controlled helminth, as immunity reduces the net outcome of climate

40 risk of infection with the soil-transmitted helminths Ascaris lumbricoides, hookworm (Ancylostoma du

41 Current deworming programs might remove this helminth-associated protective effect.

42 hosts experienced higher infections of this helminth at an earlier age during critical months in the

43 icle, we show that, in response to parasitic helminths, Batf(-/-) mice are unable to generate follicu

44 ts with an effective immune response against helminths can be more susceptible to allergy.

45 Conversely, many helminths can cause allergic-type inflammation, includin

46 hese observations led us to hypothesize that helminths can regulate GVHD and maintain GVT in mice.

47 Helminths cause chronic infections and affect the immune

48 also observed in a model of gastrointestinal helminth clearance.

49 Together, our data indicate that helminth coinfection induces arginase-1-expressing type

50 required to reverse the negative effects of helminth coinfection on the CD8 T cell response.

51 Human studies suggest that helminth coinfections contribute to increased TB suscept

52 n levels in pregnant HIV-infected women with helminth coinfections receiving ART.

53 environment, such as decreased prevalence of helminth colonization and alterations to the gut microbi

54 mposition of the bacterial microbiota affect helminth colonization and persistence within mammalian h

55 Mass deworming for soil-transmitted helminths compared with controls led to little to no imp

56 hown to clear the transmissible stage of the helminth completely in treated individuals.

57 Protection against helminths consists of adaptive responses by TH2 cells an

58 Neglected tropical diseases (NTDs) caused by helminths constitute some of the most common infections

59 gement can help to guide the optimization of helminth control strategies.

60 broad family of heme-binding proteins (MF6p/helminth defense molecules (HDMs)).

61 these studies and discuss how helminths and helminth-derived molecules may modulate these physiologi

62 s of helminth infection or administration of helminth-derived molecules on chronic inflammatory disea

63 The results show that helminth-derived products can powerfully induce regulato

64 achievement of immunological tolerance using helminth-derived products is also an exciting future pro

65 Injection of obese mice with recombinant helminth-derived Schistosoma mansoni egg-derived omega1

66 d investigation of the potential benefits of helminth-derived therapies for the prevention or treatme

67 obal and regional human disease burden of 10 helminth diseases and toxoplasmosis that may be attribut

68 filariasis and onchocerciasis are parasitic helminth diseases, which cause severe morbidities such a

69 and Drug Administration (FDA)-approved anti-helminth drug nitazoxanide (NTZ) on mitochondrial respir

70 d to be active in house dust mite (HDM)- and helminth-elicited Il4(gfp+)alphabeta(+)CD4(+) TH2 cells

71 Among women in the helminth-endemic region of the Peruvian Amazon, those wi

72 Additionally, we show that individuals from helminth-endemic regions harbor a similar protective mic

73 Helminths exploit intrinsic regulatory pathways of the m

74 urvey to test the hypothesis that in heavily helminth-exposed fishing villages on Lake Victoria, Ugan

75 Zoonotic helminth exposure in Norway was less frequent in offspri

76 Changes in response to helminth exposure may provide insights into the increase

77 While RELMalpha (Retnla) impairs helminth expulsion by inhibiting protective Th2 immunity

78 ces, and is designed specifically to support helminth genomic research.

79 able variation in their capacity to suppress helminth growth by two orders of magnitude.

80 Drug screening against helminths has often been phenotypic and typically involv

81 Although helminths have been used therapeutically to ameliorate i

82 Parasitic helminths have coexisted with human beings throughout ti

83 Helminths have strong immunoregulatory properties that m

84 In a murine colitis model, the helminth Heligmosomoides polygyrus bakeri prevents colit

85 Mice infected with the helminth Heligmosomoides polygyrus displayed increased l

86 g1b(-/-) mice failed to expel the intestinal helminths Heligmosomoides polygyrus or Nippostrongylus b

87 Acute GVHD was induced in helminth (Heligmosomoides polygyrus)-infected or uninfec

88 iota at the site of infection by a parasitic helminth (hookworm) and gluten-dependent inflammation in

89 n cytokine production and contribute to anti-helminth immunity, maintaining mucosal tissue integrity,

90 ng a previously overlooked mechanism of anti-helminth immunity.

91 In this study, we show that the helminth immunomodulator AvCystatin, a cysteine protease

92 ic effects of infections by parasitic worms (helminths) in some inflammatory disorders, such as infla

93 ed primarily to defend against extracellular helminths, in part through the co-opting of tissue repai

94 2 Ags such as alum-precipitated proteins and helminths induce IgG1, whereas Th1 Ags, such as Salmonel

95 could be important mechanisms through which helminths induce regulatory DCs that limit colitis.

96 This clarifies a relationship in which helminth-induced CD4(+) T cells disrupt M. tuberculosis

97 oinfected mice recapitulated the spectrum of helminth-induced effects on the polyclonal CD8 T respons

98 this study is the first to report a role for helminth-induced IL-5 and IL-33 in protection against au

99 tion with important clinical significance in helminth-induced immunomodulation and sepsis.

100 hRetn promoted helminth-induced immunomodulation, with increased surviv

101 autoimmunity to the suppressive activity of helminth-induced regulatory T cells (Tregs) or Th2 cells

102 s on the CD8 T cell response, we demonstrate helminth-induced suppression of IL-12-dependent differen

103 s on the CD8 T cell response, we demonstrate helminth-induced suppression of IL-12-dependent differen

104 They play a crucial role during allergy and helminth-induced Th2 responses.

105 Helminths infect more than a quarter of the world's popu

106 We show that levels of IgE-tp are raised in helminth-infected donors, and that both the classical fo

107 Helminth-infected individuals possess a higher risk of d

108 were all significantly higher in children of helminth-infected mothers, compared with children of uni

109 = .04) (P value for interaction = .01) among helminth-infected subjects as detected by microscopy.

110 In helminth-infected subjects, treatment significantly incr

111 med involving all subjects and ad hoc in the helminth-infected subjects.

112 profile was observed in cervical fluid from helminth-infected women but not helminth-uninfected wome

113 oviding a mechanism for the observation that helminth infection advances the progression of tuberculo

114 Instead, helminth infection altered the metabolic profile of the

115 Recent studies reported that the presence of helminth infection alters the composition of the bacteri

116 ate an additional 3-way interaction in which helminth infection alters the metabolic environment of t

117 ime that NETosis occurs during natural human helminth infection and demonstrate a mechanism of NETosi

118 es, which are important both for immunity to helminth infection and in allergic disease, are currentl

119 The type 2 immune response controls helminth infection and maintains tissue homeostasis but

120 l-derived protein that is highly elevated in helminth infection and sepsis.

121 is a negative association between a chronic helminth infection and skin prick test reactivity even i

122 However, helminth infection can also be detrimental in reducing v

123 ese data demonstrate that a strictly enteric helminth infection can have remote protective antiviral

124 this study, we evaluated the effect chronic helminth infection has on allergic disease in mice previ

125 In this review, we consider how studies of helminth infection have contributed toward our expanding

126 t T helper type 2 (Th2) responses induced by helminth infection impair Th1 immune responses and there

127 differentiation and clearance of a parasitic helminth infection in mice, and also abrogates the abili

128 d insight into physiological consequences of helminth infection in small ruminants and could facilita

129 Patterns of soil-transmitted helminth infection in sub-Saharan Africa have changed an

130 We show that an ongoing helminth infection increased colonization by Salmonella

131 veloping regions, it has been suggested that helminth infection may protect humans against developing

132 rward to explain the modulatory influence of helminth infection on allergic effector responses in hum

133 have demonstrated the potential benefits of helminth infection or administration of helminth-derived

134 y and tissue repair genes in the lungs after helminth infection or in the gut after induction of coli

135 to maintain their function in the context of helminth infection or malnutrition and propose that enha

136 Concurrent helminth infection potently inhibits T cell immunity; ho

137 We find that helminth infection protects mice deficient in the Crohn'

138 investigated the effects of strictly enteric helminth infection with Heligmosomoides polygyrus on res

139 y factor in fibrotic disease associated with helminth infection, but it is unclear whether it plays a

140 at play a protective role in the response to helminth infection, but they also contribute to allergic

141 n this study, we show that during intestinal helminth infection, IL-4 derived from Tfh cells is requi

142 immune cells, traditionally associated with helminth infection, maintain adipose tissue homeostasis

143 particularly in humans and rodent models of helminth infection, points towards a multitude of intera

144 esponses that are required for resistance to helminth infection, promotion of allergic inflammation,

145 n associated with diarrhea, soil-transmitted helminth infection, trachoma, environmental enteric dysf

146 After helminth infection, tuft-cell-derived IL-25 further acti

147 cules (RELMs) are highly expressed following helminth infection, where they impact both the host and

148 a great degree of geographical overlap with helminth infection.

149 allergic reactions and host protection from helminth infection.

150 responses in 927 children of mothers without helminth infection.

151 in the reactive lymph nodes during parasitic helminth infection.

152 ed protective humoral immunity to intestinal helminth infection.

153 is a central feature of the host response to helminth infection.

154 depend on fatty acid (FA) metabolism during helminth infection.

155 ed for initiating mucosal type 2 immunity to helminth infection.

156 efence, but has not been identified in human helminth infection.

157 ation of immune homeostasis and during acute helminth infection.

158 may lead to dysregulated inflammation during helminth infection.

159 e underlying immune response to this chronic helminth infection.

160 ssion of Bcl-xL and reduced apoptosis during helminth infection.

161 and IL-37 in immune modulation in a chronic helminth infection.

162 )- and IL-13-dependent host responses during helminth infection.

163 d have defective mucosal type 2 responses to helminth infection; goblet cell hyperplasia is abrogated

164 iduals were also tested for soil-transmitted helminth infections (ie, hookworm, Ascaris lumbricoides,

165 merous animal studies have demonstrated that helminth infections ameliorate allergic diseases, clinic

166 lly significant increase in the incidence of helminth infections among heterozygous girls.

167 Most studies on the relationship between helminth infections and atopic disorders have been condu

168 unomodulation is a common feature of chronic helminth infections and mainly attributed to the secreti

169 rasitic drugs might induce diabetes, whereas helminth infections appear to afford some protection aga

170 Emerging evidence suggests that helminth infections are associated with lower insulin re

171 Helminth infections are known to modulate cytokine respo

172 strong type 2 immune responses they induce, helminth infections can suppress allergy through regulat

173 Immunity to intestinal helminth infections has been well studied, but the mecha

174 In cross-sectional studies, chronic helminth infections have been associated with immunologi

175 Helminth infections have been suggested to impair the de

176 of lymphatic filariasis and soil-transmitted helminth infections in Republic of the Congo.

177 children of mothers who tested positive for helminth infections in the last trimester of pregnancy t

178 Helminth infections inhibit host immunity against microb

179 human studies indicate that definitive host helminth infections may confer protection from allergies

180 Intestinal helminth infections occur predominantly in regions where

181 Immunity to intestinal helminth infections requires the rapid activation of T h

182 trasts with the responses to other parasitic helminth infections that promote rapid Foxp3(+) Treg cel

183 Gastro-intestinal helminth infections trigger the release of interleukin-3

184 Helminth infections were ascertained by stool, urine and

185 Antenatal maternal helminth infections were not associated with reduced ant

186 d fishing villages on Lake Victoria, Uganda, helminth infections would be inversely associated with a

187 istribution and dynamics of soil-transmitted helminth infections, and yet host immunity can also infl

188 able, the danger of transplantation-mediated helminth infections, exacerbated by coincident immunosup

189 contributing to the carcinogenicity of these helminth infections, including roles for metabolites of

190 nd temporal distribution of soil-transmitted helminth infections, including the number of infected pe

191 In helminth infections, macrophages are an important source

192 factor is the presence of maternal antenatal helminth infections, which can modulate the infant's dev

193 ettings, including allergic inflammation and helminth infections.

194 flammation in many type 2 settings including helminth infections.

195 zation to microbiome changes associated with helminth infections.

196 the anti-inflammatory effector cells during helminth infections.

197 ance and disease-tolerance mechanisms during helminth infections.

198 ifferent cell types respond to bacterial and helminth infections: Salmonella infection caused an incr

199 s, neuroschistosomiasis and soil-transmitted helminths) infections.

200 ies with sewage-contaminated water supplies, helminth infestations, bare footedness, and poor housing

201 utionary conserved mechanism of host-microbe-helminth interactions.

202 r of the interactions occurring at the snail-helminth interface.

203 or more sensitive diagnostics for intestinal helminths is well known, the cost of developing and impl

204 has been well studied, but the mechanism of helminth killing prior to expulsion remains unclear.

205 -derived Pla2g1b as an essential mediator of helminth killing, highlighting a previously overlooked m

206 ten targets the motility of tissue-migrating helminth larvae, which ideally should be mimicked by ant

207 erestingly, these studies have described how helminths may alter the intestinal microbiota, potential

208 Thus, helminths may have important effects on human fertility

209 hypothesized that immune responses evoked by helminths may modify malaria-specific immune responses a

210 may represent a mechanism by which parasitic helminths may restore intestinal immune homeostasis and

211 hat have contributed to current knowledge of helminth-microbiota interactions in species of veterinar

212 ese data reveal a novel mechanism by which a helminth-modified metabolome promotes susceptibility to

213 de new insights into the mechanisms by which helminths modulate human immune responses.

214 We present evidence that helminths modulate the function and phenotype of these i

215 ease (CeD); however, the mechanisms by which helminths modulate the immune response of the human host

216 Trematode.net is an independent component of Helminth.net and currently hosts data from 16 species, w

217 n during infection with the gastrointestinal helminth Nippostrongylus brasiliensis Our results identi

218 tokines IL-25 and IL-33 or infected with the helminth Nippostrongylus brasiliensis to induce innate t

219 ector functions following infection with the helminth Nippostrongylus brasiliensis.

220 crease in the intensity of infection for the helminth not regulated by immunity.

221 caused by a chronic infection with parasitic helminths of the genus Schistosoma.

222 ondii, to investigate the negative impact of helminthes on the CD8 T cell response, we demonstrate he

223 ondii, to investigate the negative impact of helminthes on the CD8 T cell response, we demonstrate he

224 in mice have linked the protective effect of helminths on autoimmunity to the suppressive activity of

225 onship between infection with the fish-borne helminth Opishorchis felineus and specific IgE, skin pri

226 rs, with mass deworming for soil-transmitted helminths or schistosomiasis (alone or in combination wi

227 ongyloides stercoralis is a soil-transmitted helminth organism that infects ~50 to 100 million people

228 FhHDM-1, a 68-mer peptide secreted by the helminth parasite Fasciola hepatica, ameliorated disease

229 ppears to be the most economically important helminth parasite for small ruminant production in many

230 hus contortus is arguably the most injurious helminth parasite for small ruminants.

231 Helminth parasite infections are associated with a batte

232 ce exposed to two different Th2 stimuli: the helminth parasite Nippostrongylus brasiliensis (Nb) and

233 ctive juvenile stage of Fasciola hepatica, a helminth parasite of medical and veterinary importance.

234 he lung and increased ability to expulse the helminth parasite, Nippostrongylus brasiliensis These re

235 models for the impacts of climate change on helminth parasites and other pathogens of Arctic wildlif

236 or the development of protective immunity to helminth parasites but also cause the inflammation assoc

237 Helminth parasites defy immune exclusion through sophist

238 Helminth parasites have been reported to have beneficial

239 humans have demonstrated that infection with helminth parasites is associated with a reduced risk of

240 Infection by helminth parasites is associated with amelioration of al

241 strate how the immune response engendered by helminth parasites modulates Mtb-specific responses in h

242 Helminth parasites provoke multicellular immune response

243 Helminth parasites secrete molecules that potently modul

244 Gastrointestinal helminth parasites share their habitat with a myriad of

245 plex interactions among intestinal microbes, helminth parasites, and the host immune system allows fo

246 ndent amplification following infection with helminth parasites, owing to direct differentiation of e

247 re enhanced in Batf3(-/-) mice responding to helminth parasites.

248 en concurrently infected with plasmodium and helminth parasites.

249 Helminth parasitic infections are a major global health

250 , induce neutrophilic responses to the human helminth pathogen Onchocerca volvulus.

251 range of diseases caused by gastropod-borne helminths, predominantly flatworms and roundworms, whose

252 y inhibits T cell immunity; however, whether helminthes prevent T cell priming or skew clonal recruit

253 mers of A1AT protect IgE from degradation by helminth proteases may explain why these common and norm

254 hRetn in sepsis, or whether hRetn influences helminth protection against sepsis, is unknown.

255 between molecular features of allergens and helminth proteins that induce an IgE response in the hum

256 elial cells can impair larval development in helminths, providing a novel mechanism contributing to i

257 Immunity against parasitic helminths requires M2 cells and IL-13, secreted by CD4(+

258 The determinants of helminth resistance are not well understood.

259 2 innate lymphoid cells (ILC2s) promote anti-helminth responses and contribute to allergies.

260 A murine helminth/RSV coinfection model was developed.

261 Infection of mammals by the parasitic helminth Schistosoma mansoni induces antibodies to glyca

262 gnature was evident in DCs responding to the helminth Schistosoma mansoni or the allergen house dust

263 Host suppression of helminth somatic growth may be an important immune strat

264 the availability of infective stages of both helminth species and the proportional increase in the in

265 And why is infection with only a few helminth species carcinogenic?

266 Several helminth species do not have an obligatory lung migrator

267 consistent with previous reports using other helminth species in humans and animal models.

268 We used time-series data from two helminth species of a natural herbivore and investigated

269 Helminth-specific and nonspecific whole-blood cytokine r

270 cer incidence and burden of soil-transmitted helminths (STH) is hypothesized to explain the excess in

271 cycles of schistosomes and soil-transmitted helminths (STHs) suggest that water, sanitation, and hyg

272 pical diseases, such as the soil-transmitted helminths (STHs), needs to rapidly expand to meet WHO's

273 vironmental transmission of soil-transmitted helminths (STHs), which infect 1.5 billion people worldw

274 onesia, an area endemic for soil-transmitted helminths (STHs).

275 given in a targeted (n = 467; treatment when helminth stool screening was positive) or nontargeted (n

276 The host defence against helminths such as Nippostrongylus brasiliensis is orches

277 However, zoonotic helminths, such as Toxocara species (spp.), have been as

278 Nevertheless, reversal of helminth suppression of the innate IL-12 response of CD8

279 arasites modulates Mtb-specific responses in helminth-TB coinfection.

280 stronger correlate of infection outcomes for helminths than host species traits.

281 noply of immunomodulatory mechanisms used by helminths, their potential utility in human disease, and

282 stigations have highlighted the potential of helminth therapy for treating a range of inflammatory di

283 diminuta, unlike other parasites assessed as helminth therapy, causes no host tissue damage while pot

284 ive T helper cell type 2 immune responses to helminths, ticks, and certain other parasites.

285 The ability of intestinal helminths to reduce DTH responses may have clinical impl

286 This trial shows the capacity of helminths to up-regulate inhibitory molecules and to sup

287 Helminths trigger multiple immunomodulatory pathways tha

288 l fluid from helminth-infected women but not helminth-uninfected women.

289 ae, which ideally should be mimicked by anti-helminth vaccines.

290 Protozoa and helminths, vector-borne, foodborne, soilborne and waterb

291 trong evidence that individuals with certain helminths were more prone to atopy in this setting.

292 d, whereas others, such as certain parasitic helminths, were highly localised.

293 eported that Nippostrongylus brasiliensis, a helminth with a lung migratory phase, affected host resi

294 ETATION: Mass deworming for soil-transmitted helminths with or without deworming for schistosomiasis

295 fects of mass deworming for soil-transmitted helminths (with or without deworming for schistosomiasis

296 translated in vivo into better clearance of helminth worm infection in mice.

297 Parasitic helminth worms, such as Schistosoma mansoni, are endemic

298 2 billion people worldwide are infected with helminths (worms).

299 ase) is known to be induced by allergens and helminths, yet its role in immunity is unclear.

300 rol for schistosomiasis and soil-transmitted helminths, yet the World Health Organization recently re